Quantum dots enhance Cu<sup>2+</sup>-induced hepatic l02 cells toxicity: involvement of Nrf2

Zhao, Yijiao; Lin, Kuangfei

doi:10.1080/02772240903503955

Cited by 2 publications

References 19 publications

(27 reference statements)

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Extrahepatic Drug‐Metabolizing Enzymes and Their Significance

Jhajra

Varkhede

Ahire

et al. 2012

Encyclopedia of Drug Metabolism and Interactions

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Drug‐metabolizing enzymes (DMEs) are primarily expressed in the liver but their role in the extrahepatic tissues such as gastrointestinal tract (GIT), pulmonary, excretory, nervous, cardiovascular system, and skin cannot be neglected. Generally, the expression of DMEs in extrahepatic tissues is quantitatively lower than that in the liver, but there are a few enzymes such as CYP1A1, CYP1B1, CYP2F1, and CYP2U1 that are more abundant in extrahepatic organs. As many extrahepatic organs are portals for administered drugs, DMEs expressed in these organs can be responsible for significant metabolism, leading to first‐pass effects and lower bioavailability. Extrahepatic DMEs are also involved in bioactivation of prodrugs and formation of reactive metabolites that may interact with cellular components, resulting in organ‐specific toxicity. Activity and expression of extrahepatic DMEs is often altered by coadministered drugs, leading to drug–drug interactions. Expression of DMEs in living beings affected by a host of environmental and genetic factors such as genetic polymorphism, age, gender, pathophysiological conditions, inborn errors in metabolism, food habits, and environmental pollutants, contributing to varied drug effects and idiosyncratic toxicities.

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Extrahepatic Drug‐Metabolizing Enzymes and Their Significance

Jhajra

Varkhede

Ahire

et al. 2012

Encyclopedia of Drug Metabolism and Interactions

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Research Advances on Apoptosis Caused by Quantum Dots

Zhan

Tang

2014

Biol Trace Elem Res

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Recently, quantum dots (QDs) have been widely applied in biological and biomedical fields such as cell labeling, living tissue imaging, and photodynamic therapy because of their superior optical properties. Meanwhile, the potential biological negative effects and/or toxic effects of QDs have become increasingly important, especially the cytotoxicity caused by QDs. One of the common cytotoxicity when living organisms are treated with QD is apoptosis, where many attempts have been made to explain the mechanisms of apoptosis caused by QDs' use. One of the mechanisms is the production of cadmium ion (Cd(2+)) and reactive oxygen species (ROS). Excess generation of ROS will result in oxidative stress that would mediate apoptosis. Furthermore, the activation of cell death receptors and mitochondria-dependent such as B cell lymphoma 2 (Bcl-2) family and the caspase family could onset apoptosis. Signal transduction such as some classical signal pathways of PI3K-AKT, NF-E2-related factor 2 (Nrf2)-antioxidant response element (ARE), mitogen-activated protein kinases (MAPKs), and nuclear factor kappa B (NF-κB) also plays an important role in the regulation of apoptosis. Several ways to reduce the apoptotic rate have been introduced, such as surface modification, controlling, the dose, size, and exposure time of QDs as well as using antioxidants or inhibitors. In this review, we attempted to review the most recent findings associated with apoptosis caused by QDs so as to provide some guidelines for a safer QD application in the future.

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Quantum dots enhance Cu²⁺-induced hepatic l02 cells toxicity: involvement of Nrf2

Cited by 2 publications

References 19 publications

Extrahepatic Drug‐Metabolizing Enzymes and Their Significance

Extrahepatic Drug‐Metabolizing Enzymes and Their Significance

Research Advances on Apoptosis Caused by Quantum Dots

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Quantum dots enhance Cu2+-induced hepatic l02 cells toxicity: involvement of Nrf2

Cited by 2 publications

References 19 publications

Extrahepatic Drug‐Metabolizing Enzymes and Their Significance

Extrahepatic Drug‐Metabolizing Enzymes and Their Significance

Research Advances on Apoptosis Caused by Quantum Dots

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Quantum dots enhance Cu²⁺-induced hepatic l02 cells toxicity: involvement of Nrf2